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The protein alpha-synuclein is abundant in healthy brains and plays an important role in enabling communication between nerve cells. However, under certain conditions, misfolded alpha-synuclein proteins can accumulate into toxic clumps inside neurons. Known as Lewy bodies, these clusters of proteins are a hallmark of Parkinson's disease and some forms of dementia.

In recent years, researchers have discovered that these misfolded proteins don't just stay in one place: They spread from one cell to another through the fluid spaces of the brain.

"Once it starts piling up in one neuron and causing disease, it can get out of cell one and get into cell two," says Stephen Strittmatter, M.D., Ph.D., Vincent Coates professor of neurology and professor and chair of neuroscience. "And so it spreads through the brain."

In a new team science project funded by Aligning Science Across Parkinson's (ASAP), Yale School of Medicine researchers hope to shed new light on what happens to alpha-synuclein between nerve cells—and what determines where it ends up.

"What is its fate?" Strittmatter asks. "What is the balance between moving it out of the brain versus being taken up into another neuron and spreading disease?"

To try to find that balance, Strittmatter and colleagues plan to approach the problem from different angles.

The first step in this work was to determine which proteins in the nerve cells were responsible for attaching to and picking up the misfolded alpha-synuclein.

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